Plasminogen Activator Inhibitor-1 as a Marker of Thrombosis among Prehypertensive Patients: A Cross-sectional Study

Introduction: Impaired endogenous fibrinolysis has been shown to play a role in the pathogenesis and complications of hypertension. Plasminogen Activator Inhibitor-1 (PAI-1) is said to be a predictor of impaired fibrinolysis and thrombosis. Prehypertension is a common worldwide condition and is known to be an independent risk factor for Cardiovascular Disease (CVD). Aim: Present study aimed to measure plasma PAI-1 levels in prehypertensive patients and normal subjects and to find the correlation between elevated PAI-1 levels with Blood Pressure (BP), triglycerides, total cholesterol, Low-Density Lipoproteins (LDL) cholesterol, High-Density Lipoproteins (HDL) cholesterol, and urine albumin. Materials and Methods: This cross-sectional analytical study included 100 patients, comprising 50 prehypertensive individuals and 50 controls, aged between 35 and 50 years. The study was conducted at Sapthagiri Institute of Medical Sciences and Research Centre in Bangalore, India. Anthropometric measurements, PAI-1 levels, total cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), and urine albumin were measured using standard procedures. The data were statistically analysed using the Statistical Package for Social Sciences (SPSS) version 10.0, applying Student t-test and Chisquare test. Correlation analysis was performed to assess the relationship between PAI-1 and various parameters. Results: A total of 100 patients were included in the study which had 64 men and 36 women with a mean age of 46±7 years. PAI-1 levels were significantly higher in the prehypertensive group compared to the control group (p-value=0.013). Participants with higher plasma PAI-1 levels had significantly elevated BP (p-value=0.001) compared to those with lower PAI-1 levels. Total cholesterol, triglycerides, and LDL cholesterol were significantly increased in prehypertensive individuals (p-value=0.001), whereas HDL cholesterol was significantly lower (p-value=0.001). The study also observed a significant increase in urine albumin in the prehypertensive group with elevated PAI-1 levels compared to the controls (p-value=0.001). The study revealed that elevated plasma PAI-1 levels did not show a significant positive correlation with SBP and DBP (r=0.138 and 0.660, p-value of 0.338 and 0.648, respectively). Plasma PAI-1 levels were weakly correlated with total cholesterol (r=0.145, p-value 0.315), LDL cholesterol (r=-0.068, p-value 0.640), HDL cholesterol (r=0.21, p-value 0.882), and triglycerides (r=0.207, p-value 0.150). There was no significant correlation between increased PAI-1 levels and urine albumin (r=-0.225, p-value of 0.117). Conclusion: Present study demonstrated that plasma PAI-1, total cholesterol, triglycerides, LDL cholesterol, and urine albumin were significantly elevated in prehypertensive individuals, suggesting vascular damage and inflammation. As prehypertension is often asymptomatic, patients with prehypertension should be considered to have an increased risk for CVD.